Malaria is an infectious disease caused by the protozoan parasites belonging to Plasmodium genus and is transmitted to mammalian hosts through the bite of infected mosquitoes. Four species of Plasmodium are pathogenic in humans: P. vivax, P. malariae, P. ovale, and P. falciparum. Several other species of Plasmodium infect animals. According to the latest report from WHO, 214 million cases of malaria were reported in 2015 and led to 438000 deaths. Since, malaria is concentrated in countries with comparatively low national income; the cost of malaria treatment is disproportionately borne by the most resource-constrained countries. Although treatment is available, the development of drug resistance poses a big problem in current malaria treatment. Resistance to artemisinins has now been detected in five countries. The most severe neurological complication of malarial infection is cerebral malaria. It is fatal if untreated and is considered as a leading cause of neuro-disability in African children.
The parasitic protozoan Toxoplasma gondii is the etiologic agent for toxoplasmosis, a parasitic disease widespread among various warm-blooded animals. Treatment options for Toxoplasma include antibiotics such as clindamycin or pyrimethamine/sulphadoxin combination, but the effectiveness of these against the cyst form of the parasite in still not clear and hence it is quite difficult to clear infection completely from infected individuals. It is estimated that ˜30% of the global population is infected by this pathogen, and is transmitted via the oral route by consumptions of contaminated food and water. When mammalian hosts eat infected food (rare cooked meat in case of humans), or drink oocysts contaminated water, they acquire the infection [Harker K S, Ueno N, Lodoen M B. Toxoplasma gondii dissemination: a parasite's journey through the infected host. Parasite Immunol. 2015, 37(3): 141-9]. Clinical symptoms associated with Toxoplasma infection vary from severe (congenital encephalopathy in neonates) to mild (self limiting fever in healthy adults). Recent reports have also suggested that chronic toxoplasmosis in humans can result in altered neurological functions due to the presence of cyst form of the parasite in brain.
WO 2006117552 A1 discloses compound of formula (IA) or (IB), or a salt, N-oxide, hydrate or solvate thereof:

Wherein, Y1 is a bond, —C(═O)—, —S(═O)2—, —C(O)O—, —C(O)NR3—, —C(═S)NR3, —C(═NH)NR3 or —S(O)2NR3— wherein R3 is hydrogen or optionally substituted C1-C6 alkyl; L1 is a divalent radical of formula -(Alk1)m(Q1)n(Alk2)p- wherein m, n and p are independently O or 1, Q1 is (i) an optionally substituted divalent mono- or bicyclic carbocyclic or heterocyclic radical having 5-13 ring members, or (ii), in the case where p is O, a divalent radical of formula -Q2-X2— wherein X2 is O—, —S— or NRA— wherein RA is hydrogen or optionally substituted C1-C3 alkyl, and Q2 is an optionally substituted divalent mono- or bicyclic carbocyclic or heterocyclic radical having 5-13 ring members, AIk1 and AIk2 independently represent optionally substituted divalent C3-C7 cycloalkyl radicals, or optionally substituted straight or branched, C1-C6 alkylene, C2-C6 alkenylene, or C2-C6 alkynylene radicals which may optionally contain or terminate in an ether (—O—), thioether (—S—) or amino (—NRA—) link wherein RA is hydrogen or optionally substituted C1-C3 alkyl; z is 0 or 1; R6 is C1-C4 alkoxy, hydrogen or halo; W represents a bond, —CH2—, O, S, S(═O)2—, or —NR5— where R5 is hydrogen or C1-C4 alkyl; Q is ═N—, ═CH— or ═C(X1)— wherein X1 is cyano, cyclopropyl or halo; each L2 independently represents a radical of formula ˜(Alk3)a-Z-(Alk4)b- wherein a and b are independently 0 or 1; AIk3 and AIk4 independently represent optionally substituted divalent C3-C7 cycloalkyl radicals, or optionally substituted straight or branched, C1-C6 alkylene, C2-C6 alkenylene, or C2-C6 alkynylene radicals which may optionally contain or terminate in an ether (—O—), thioether (—S—) or amino (—NRA—) link wherein RA is hydrogen or optionally substituted C1-C3 alkyl; Z represents a bond or an —O—, —S—, —S(═O)2—, —C(═O)—, —NRB—, —CONRB—, —NR6CO—, —SO2NR6—, NR6SO2—, —NR6CONR6— or —NR6CSNR6— radical, wherein R6 is hydrogen or C1-C3 alkyl;
r and s are independently O or 1; and rings A, B and C are mono- or bi-cyclic carbocyclic or heterocyclic rings or ring systems having up to 12 ring atoms;
R is a radical of formula (X) or (Y):

Wherein Ri is a carboxylic acid group (—COOH), or an ester group which is hydrolysable by one or more intracellular carboxylesterase enzymes to a carboxylic acid group; R4 is hydrogen; or optionally substituted C1-C6 alkyl, C3-C7 cycloalkyl, aryl, aryl(d-C6 alkyl)-, heteroaryl, heteroaryl(CrC6 alkyl)-, —(C═O)R3, —(C═O)OR3, or —(C═O)NR3 wherein R3 is hydrogen or optionally substituted (Ci-C6)alkyl, C3-C7 cycloalkyl, aryl, 317!(C1-C6 alkyl)-, heteroaryl, or heteroaryl(CrC6 alkyl)-; R41 is hydrogen or optionally substituted C1-C6 alkyl; and D is a monocyclic heterocyclic ring of 5 or 6 ring atoms wherein R1 is linked to a ring carbon adjacent the ring nitrogen shown, and ring D is optionally fused to a second carbocyclic or heterocyclic ring of 5 or 6 ring atoms in which case the bond shown intersected by a wavy line may be from a ring atom in said second ring.
CA 2918888 A1 discloses compound represented by general formula I, has a strong Ax1 inhibiting activity by introducing a distinctive bicyclic structure in which a saturated carbocyclic ring is fused to a pyridone ring, and thus may be used as a therapeutic agent for Ax1 related diseases such as acute myeloid leukemia, melanoma, breast cancer, pancreatic cancer, cancer such as glioma, kidney disease, immune system disease, and circulatory system disease. Further, it discloses that L is —CO—.

US 20090312313 A1 provides compounds represented by formula (I) and pharmaceutically acceptable salts and solvates thereof:
wherein X represents CH or N; Z represents —O—, —NH— or —C(═O)—; R and R′ represent a hydrogen atom, hydroxyl, a halogen atom, optionally substituted alkyl, optionally substituted alkenyl optionally substituted alkoxy, amino, aminocarbonyl, or an optionally substituted heterocyclic group; and A represents an optionally substituted specific carbocyclic or heterocyclic group. The compounds according to the present invention have excellent TGFβ inhibitory activity.
WO 2007146824 A2 discloses compounds of Formula (I), and stereoisomers, geometric isomers, tautomers, solvates, metabolites, salts and pharmaceutically acceptable prodrugs thereof, are useful for inhibiting receptor tyrosine kinases and for treating hyperproliferative disorders mediated thereby. Methods of using compounds of Formula (I), and stereoisomers, geometric isomers, tautomers, solvates and pharmaceutically acceptable salts thereof, for in vitro, in situ, and in vivo diagnosis, prevention or treatment of such disorders in mammalian cells, or associated pathological conditions are disclosed.

U.S. Pat. No. 6,809,097 B1 discloses compounds of the formula (I):
wherein: R2 represents hydroxy, halogeno, C1-3alkyl, C1-3alkoxy, C1-3alkanoyloxy, trifluoromethyl, cyano, amino or nitro; n is an integer from 0 to 5; Z represents —O—, —NH—, —S— or —CH2—; G1 represents phenyl or a 5-10 membered heteroaromatic cyclic or bicyclic group; Y1, Y2, Y3 and Y4 each independently represents carbon or nitrogen; R1 represents fluoro or hydrogen; m is an integer from 1 to 3; R3 represents hydrogen, hydroxy, halogeno, cyano, nitro, trifluoromethyl, C1-3 alkyl, —NR4R5 (wherein R4 and R5, can each be hydrogen or C1-3alkyl), or a group R6—X1— wherein X1 represents —CH2— or a heteroatom linker group and R6 is an alkyl, alkenyl or alkynyl chain optionally substituted by for example hydroxy, amino, nitro, alkyl, cycloalkyl, alkoxyalkyl, or an optionally substituted group selected from pyridone, phenyl and a heterocyclic ring, which alkyl, alkenyl or alkynyl chain may have a heteroatom linker group, or R6 is an optionally substituted group selected from pyridone, phenyl and a heterocyclic ring and salts thereof, in the manufacture of a medicament for use in the production of an antiangiogenic and/or vascular permeability reducing effect in warm-blooded animals such as humans, processes for the preparation of such derivatives, pharmaceutical compositions containing a compound of formula I or a pharmaceutically acceptable salt thereof as active ingredient and compounds of formula I. The compounds of formula I and the pharmaceutically acceptable salts thereof inhibit the effects of VEGF, a property of value in the treatment of a number of disease states including cancer and rheumatoid arthritis.
WO 2009036412 A1 relates to modulators of ATP-Binding Cassette (‘ABC’) transporters or fragments thereof, including Cystic Fibrosis Transmembrane Conductance Regulator, compositions thereof, and methods therewith. The present invention also relates to methods of treating ABC transporter mediated diseases using such modulators.

U.S. Pat. No. 4,492,704 A relates to a class of quinoline quinones, which are useful for the therapy of immediate hypersensitivity reactions, such as asthma, and in treating any condition characterized by excessive release of leukotrienes. This patent also includes a method for treating these conditions, which comprises administering to animals, including humans, an effective dose of the quinoline quinone compounds. A further part of this patent is pharmaceutical formulations containing these pharmacologically-active compounds.

Article titled, “Synthesis, Characterization, and Pharmacological Evaluation of Silicon-Containing Aminoquinoline Organometallic Complexes As Antiplasmodial, Antitumor, and Antimycobacterial Agents” by Yiqun Li, Carmen de Kock, Peter J. Smith, Hajira Guzgay, Denver T. Hendricks, Krupa Naran, Valerie Mizrah, Digby F. Warner, Kelly Chibale, and Gregory S. Smith in Organometallics, 2013, 32 (1), pp 141-150 reports two silicon-containing analogues (1, 2) of chloroquine, modified in the lateral side chain with organosilicon moieties, were synthesized. Compounds 1 and 2 were further reacted with dinuclear half-sandwich transition metal precursors [Ru(Ar)(μ-Cl)Cl]2 (Ar=η6-p-iPrC6H4Me; η6-C6H6; η6-C6H5OCH2CH2OH), [Rh(COD)(μ-Cl)]2, and [RhCp*(μ-Cl)Cl]2, to yield a series of neutral mononuclear Ru(II), Rh(I), and Rh(III) silicon-aminoquinoline complexes (3-12). Compounds 1 and 2 act as monodentate donors that coordinate to the transition metals via the quinoline nitrogen of the aminoquinoline scaffold. Furthermore, the in vitro pharmacological activities of compounds 1-12 were established against chloroquine-sensitive (NF54) and chloroquine-resistant (Dd2) strains of the malarial parasite Plasmodium falciparum and against the pathogenic bacterium Mycobacterium tuberculosis H37Rv, as well as an esophageal (WHCO1) cancer cell line.
The search for new anti-malarial drugs is still in progress. However, the hope that new drugs would help eradicate the disease has not been realized. Accordingly, there is a need in the art for new treatments for effectively combating malaria, and particularly malarial forms that are resistant to current treatments, but without the side-effects and complications of drugs and treatments that are presently available. Also there is an urgent need for new and effective drugs for treating and preventing chronic toxoplasmosis.